Parental and sexual conflicts over the Peg3 imprinted domain
In the current study, the imprinting control region of the mouse Peg3 domain was deleted to test its functional impact on animal growth and survival. The paternal transmission of the deletion resulted in complete abolition of the transcription of two paternally expressed genes, Peg3 and Usp29 , caus...
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| Veröffentlicht in: | Scientific reports 2016-11, Vol.6 (1), p.38136-38136, Article 38136 |
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| creator | He, Hongzhi Perera, Bambarendage P. U. Ye, An Kim, Joomyeong |
| description | In the current study, the imprinting control region of the mouse
Peg3
domain was deleted to test its functional impact on animal growth and survival. The paternal transmission of the deletion resulted in complete abolition of the transcription of two paternally expressed genes,
Peg3
and
Usp29
, causing the reduced body weight of the pups. In contrast, the maternal transmission resulted in the unexpected transcriptional up-regulation of the remaining paternal allele of both
Peg3
and
Usp29
, causing the increased body weight and survival rates. Thus, the imprinted maternal allele of the ICR may be a suppressor antagonistic to the active paternal allele of the ICR, suggesting a potential intralocus allelic conflict. The opposite outcomes between the two transmissions also justify the functional compromise that the maternal allele has become epigenetically repressed rather than genetically deleted during mammalian evolution. The mice homozygous for the deletion develop normally but with a skewed sex ratio, one male per litter, revealing its sex-biased effect. Overall, the
Peg3
locus may have evolved to an imprinted domain to cope with both parental and sexual conflicts driven by its growth-stimulating paternal versus growth-suppressing maternal alleles. |
| doi_str_mv | 10.1038/srep38136 |
| format | Article |
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Peg3
domain was deleted to test its functional impact on animal growth and survival. The paternal transmission of the deletion resulted in complete abolition of the transcription of two paternally expressed genes,
Peg3
and
Usp29
, causing the reduced body weight of the pups. In contrast, the maternal transmission resulted in the unexpected transcriptional up-regulation of the remaining paternal allele of both
Peg3
and
Usp29
, causing the increased body weight and survival rates. Thus, the imprinted maternal allele of the ICR may be a suppressor antagonistic to the active paternal allele of the ICR, suggesting a potential intralocus allelic conflict. The opposite outcomes between the two transmissions also justify the functional compromise that the maternal allele has become epigenetically repressed rather than genetically deleted during mammalian evolution. The mice homozygous for the deletion develop normally but with a skewed sex ratio, one male per litter, revealing its sex-biased effect. Overall, the
Peg3
locus may have evolved to an imprinted domain to cope with both parental and sexual conflicts driven by its growth-stimulating paternal versus growth-suppressing maternal alleles.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/srep38136</identifier><identifier>PMID: 27901122</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/106 ; 45/29 ; 45/43 ; 45/77 ; 631/208/176/1968 ; 631/208/199 ; Alleles ; Animal growth ; Animals ; Binding sites ; Biological Evolution ; Body weight ; DNA methylation ; Epigenesis, Genetic - genetics ; Evolution ; Female ; Females ; Gene deletion ; Gene regulation ; Genes ; Genomic imprinting ; Genomic Imprinting - genetics ; Humanities and Social Sciences ; Kruppel-Like Transcription Factors - genetics ; Male ; Males ; Mammals ; Mice ; Mice, Inbred ICR ; Mice, Knockout ; multidisciplinary ; Mutation ; Peg3 protein ; Protein Domains - genetics ; Science ; Sequence Deletion - genetics ; Sex ratio ; Sexes ; Survival ; Survival Rate ; Transcription ; Transcription, Genetic - genetics ; Ubiquitin-Specific Proteases - genetics ; Up-Regulation - genetics</subject><ispartof>Scientific reports, 2016-11, Vol.6 (1), p.38136-38136, Article 38136</ispartof><rights>The Author(s) 2016</rights><rights>Copyright Nature Publishing Group Nov 2016</rights><rights>Copyright © 2016, The Author(s) 2016 The Author(s)</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c504t-c181fb58ce08daa377bcf5a4b463e75c2b99a49ec4844739c652c976f896e56d3</citedby><cites>FETCH-LOGICAL-c504t-c181fb58ce08daa377bcf5a4b463e75c2b99a49ec4844739c652c976f896e56d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5128876/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5128876/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,725,778,782,862,883,27911,27912,41107,42176,51563,53778,53780</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27901122$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>He, Hongzhi</creatorcontrib><creatorcontrib>Perera, Bambarendage P. U.</creatorcontrib><creatorcontrib>Ye, An</creatorcontrib><creatorcontrib>Kim, Joomyeong</creatorcontrib><title>Parental and sexual conflicts over the Peg3 imprinted domain</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>In the current study, the imprinting control region of the mouse
Peg3
domain was deleted to test its functional impact on animal growth and survival. The paternal transmission of the deletion resulted in complete abolition of the transcription of two paternally expressed genes,
Peg3
and
Usp29
, causing the reduced body weight of the pups. In contrast, the maternal transmission resulted in the unexpected transcriptional up-regulation of the remaining paternal allele of both
Peg3
and
Usp29
, causing the increased body weight and survival rates. Thus, the imprinted maternal allele of the ICR may be a suppressor antagonistic to the active paternal allele of the ICR, suggesting a potential intralocus allelic conflict. The opposite outcomes between the two transmissions also justify the functional compromise that the maternal allele has become epigenetically repressed rather than genetically deleted during mammalian evolution. The mice homozygous for the deletion develop normally but with a skewed sex ratio, one male per litter, revealing its sex-biased effect. Overall, the
Peg3
locus may have evolved to an imprinted domain to cope with both parental and sexual conflicts driven by its growth-stimulating paternal versus growth-suppressing maternal alleles.</description><subject>13/106</subject><subject>45/29</subject><subject>45/43</subject><subject>45/77</subject><subject>631/208/176/1968</subject><subject>631/208/199</subject><subject>Alleles</subject><subject>Animal growth</subject><subject>Animals</subject><subject>Binding sites</subject><subject>Biological Evolution</subject><subject>Body weight</subject><subject>DNA methylation</subject><subject>Epigenesis, Genetic - genetics</subject><subject>Evolution</subject><subject>Female</subject><subject>Females</subject><subject>Gene deletion</subject><subject>Gene regulation</subject><subject>Genes</subject><subject>Genomic imprinting</subject><subject>Genomic Imprinting - genetics</subject><subject>Humanities and Social Sciences</subject><subject>Kruppel-Like Transcription Factors - genetics</subject><subject>Male</subject><subject>Males</subject><subject>Mammals</subject><subject>Mice</subject><subject>Mice, Inbred ICR</subject><subject>Mice, Knockout</subject><subject>multidisciplinary</subject><subject>Mutation</subject><subject>Peg3 protein</subject><subject>Protein Domains - genetics</subject><subject>Science</subject><subject>Sequence Deletion - genetics</subject><subject>Sex ratio</subject><subject>Sexes</subject><subject>Survival</subject><subject>Survival Rate</subject><subject>Transcription</subject><subject>Transcription, Genetic - genetics</subject><subject>Ubiquitin-Specific Proteases - genetics</subject><subject>Up-Regulation - genetics</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNplkV1LwzAYhYMobsxd-Aek4I0K0-arTUAEGX7BwF3odUjTt1tH28ykHfrvzdgcU3OTA-_DyXlzEDrF8TWOqbjxDpZUYJocoD6JGR8RSsjhnu6hofeLOBxOJMPyGPVIKmOMCemj26l20LS6inSTRx4-uyCNbYqqNK2P7Apc1M4hmsKMRmW9dGXTQh7lttZlc4KOCl15GG7vAXp_fHgbP48mr08v4_vJyPCYtSODBS4yLgzEIteapmlmCq5ZxhIKKTckk1IzCYYJxlIqTcKJkWlSCJkAT3I6QHcb32WX1ZCbENjpSoUwtXZfyupS_Z405VzN7EpxTIRIk2BwsTVw9qMD36q69AaqSjdgO6-wYJwwkTIa0PM_6MJ2rgnrBUpKmmDJWaAuN5Rx1ocGil0YHKt1LWpXS2DP9tPvyJ8SAnC1Afz6e2fg9p785_YNI22WGQ</recordid><startdate>20161130</startdate><enddate>20161130</enddate><creator>He, Hongzhi</creator><creator>Perera, Bambarendage P. 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U. ; Ye, An ; Kim, Joomyeong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c504t-c181fb58ce08daa377bcf5a4b463e75c2b99a49ec4844739c652c976f896e56d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>13/106</topic><topic>45/29</topic><topic>45/43</topic><topic>45/77</topic><topic>631/208/176/1968</topic><topic>631/208/199</topic><topic>Alleles</topic><topic>Animal growth</topic><topic>Animals</topic><topic>Binding sites</topic><topic>Biological Evolution</topic><topic>Body weight</topic><topic>DNA methylation</topic><topic>Epigenesis, Genetic - genetics</topic><topic>Evolution</topic><topic>Female</topic><topic>Females</topic><topic>Gene deletion</topic><topic>Gene regulation</topic><topic>Genes</topic><topic>Genomic imprinting</topic><topic>Genomic Imprinting - genetics</topic><topic>Humanities and Social Sciences</topic><topic>Kruppel-Like Transcription Factors - genetics</topic><topic>Male</topic><topic>Males</topic><topic>Mammals</topic><topic>Mice</topic><topic>Mice, Inbred ICR</topic><topic>Mice, Knockout</topic><topic>multidisciplinary</topic><topic>Mutation</topic><topic>Peg3 protein</topic><topic>Protein Domains - genetics</topic><topic>Science</topic><topic>Sequence Deletion - genetics</topic><topic>Sex ratio</topic><topic>Sexes</topic><topic>Survival</topic><topic>Survival Rate</topic><topic>Transcription</topic><topic>Transcription, Genetic - genetics</topic><topic>Ubiquitin-Specific Proteases - genetics</topic><topic>Up-Regulation - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>He, Hongzhi</creatorcontrib><creatorcontrib>Perera, Bambarendage P. U.</creatorcontrib><creatorcontrib>Ye, An</creatorcontrib><creatorcontrib>Kim, Joomyeong</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>He, Hongzhi</au><au>Perera, Bambarendage P. U.</au><au>Ye, An</au><au>Kim, Joomyeong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Parental and sexual conflicts over the Peg3 imprinted domain</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2016-11-30</date><risdate>2016</risdate><volume>6</volume><issue>1</issue><spage>38136</spage><epage>38136</epage><pages>38136-38136</pages><artnum>38136</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>In the current study, the imprinting control region of the mouse
Peg3
domain was deleted to test its functional impact on animal growth and survival. The paternal transmission of the deletion resulted in complete abolition of the transcription of two paternally expressed genes,
Peg3
and
Usp29
, causing the reduced body weight of the pups. In contrast, the maternal transmission resulted in the unexpected transcriptional up-regulation of the remaining paternal allele of both
Peg3
and
Usp29
, causing the increased body weight and survival rates. Thus, the imprinted maternal allele of the ICR may be a suppressor antagonistic to the active paternal allele of the ICR, suggesting a potential intralocus allelic conflict. The opposite outcomes between the two transmissions also justify the functional compromise that the maternal allele has become epigenetically repressed rather than genetically deleted during mammalian evolution. The mice homozygous for the deletion develop normally but with a skewed sex ratio, one male per litter, revealing its sex-biased effect. Overall, the
Peg3
locus may have evolved to an imprinted domain to cope with both parental and sexual conflicts driven by its growth-stimulating paternal versus growth-suppressing maternal alleles.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>27901122</pmid><doi>10.1038/srep38136</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 13/106 45/29 45/43 45/77 631/208/176/1968 631/208/199 Alleles Animal growth Animals Binding sites Biological Evolution Body weight DNA methylation Epigenesis, Genetic - genetics Evolution Female Females Gene deletion Gene regulation Genes Genomic imprinting Genomic Imprinting - genetics Humanities and Social Sciences Kruppel-Like Transcription Factors - genetics Male Males Mammals Mice Mice, Inbred ICR Mice, Knockout multidisciplinary Mutation Peg3 protein Protein Domains - genetics Science Sequence Deletion - genetics Sex ratio Sexes Survival Survival Rate Transcription Transcription, Genetic - genetics Ubiquitin-Specific Proteases - genetics Up-Regulation - genetics |
| title | Parental and sexual conflicts over the Peg3 imprinted domain |
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